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Cells
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Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II
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Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 4190

Special Issue Editor

Dr. Lon J. van Winkle

E-Mail Website
Guest Editor
1. Department of Biochemistry, Midwestern University, Downers Grove, IL 60515, USA
2. Department of Medical Humanities, Rocky Vista University, Parker, CO 80122, USA
Interests: cell physiology; cell metabolism; development; cell differentiation; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Both maternal and paternal environmental challenges and assisted reproductive technology (ART) can alter early embryo development. These molecular alterations often produce unwanted characteristics in adulthood. Included in the undesirable characteristics are metabolic syndrome, diabetes, hypertension, and other related disorders.  Strikingly, these disorders may, in many cases, exhibit transgenerational expression. A previous Special Issue, entitled "Molecular and Clinical Advances in Understanding Early Embryo Development” was very successful, and comprises 13 papers and reviews concerning various aspects of early embryo development. However,  embryo development is complicated and dynamic, making it difficult to cover in one Special Issue.

Therefore, we aim to work towards creating an additional Special Issue on this topic. In this Special Issue, we aim to explore current research concerning these and related environmental challenges to early embryos and their mothers and fathers. We invite submission of manuscripts concerning, but not limited to, the following keywords regarding early embryo development.

We are pleased to invite you to contribute original articles, reviews, communications, etc. We are looking forward to your contributions to this Special Issue.

Dr. Lon J. van Winkle
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolism
  • biomembrane transport
  • genetics
  • epigenetic modifications
  • transgenerational inheritance
  • signaling
  • ART
  • in vitro culture
  • trophectoderm
  • inner cell mass

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Related Special Issue

Published Papers (3 papers)

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Research

27 pages, 23298 KiB  
Article
Keratin 8/18a.1 Expression Influences Embryonic Neural Crest Cell Dynamics and Contributes to Postnatal Corneal Regeneration in Zebrafish
by Antionette L. Williams and Brenda L. Bohnsack
Cells 2024, 13(17), 1473; https://doi.org/10.3390/cells13171473 - 2 Sep 2024
Viewed by 782
Abstract
A complete understanding of neural crest cell mechanodynamics during ocular development will provide insight into postnatal neural crest cell contributions to ophthalmic abnormalities in adult tissues and inform regenerative strategies toward injury repair. Herein, single-cell RNA sequencing in zebrafish during early eye development [...] Read more.
A complete understanding of neural crest cell mechanodynamics during ocular development will provide insight into postnatal neural crest cell contributions to ophthalmic abnormalities in adult tissues and inform regenerative strategies toward injury repair. Herein, single-cell RNA sequencing in zebrafish during early eye development revealed keratin intermediate filament genes krt8 and krt18a.1 as additional factors expressed during anterior segment development. In situ hybridization and immunofluorescence microscopy confirmed krt8 and krt18a.1 expression in the early neural plate border and migrating cranial neural crest cells. Morpholino oligonucleotide (MO)-mediated knockdown of K8 and K18a.1 markedly disrupted the migration of neural crest cell subpopulations and decreased neural crest cell marker gene expression in the craniofacial region and eye at 48 h postfertilization (hpf), resulting in severe phenotypic defects reminiscent of neurocristopathies. Interestingly, the expression of K18a.1, but not K8, is regulated by retinoic acid (RA) during early-stage development. Further, both keratin proteins were detected during postnatal corneal regeneration in adult zebrafish. Altogether, we demonstrated that both K8 and K18a.1 contribute to the early development and postnatal repair of neural crest cell-derived ocular tissues. Full article
(This article belongs to the Special Issue Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II)
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15 pages, 3633 KiB  
Article
Proline and Proline Analogues Improve Development of Mouse Preimplantation Embryos by Protecting Them against Oxidative Stress
by Madeleine L. M. Hardy, Dheerja Lakhiani, Michael B. Morris and Margot L. Day
Cells 2023, 12(22), 2640; https://doi.org/10.3390/cells12222640 - 16 Nov 2023
Cited by 1 | Viewed by 1446
Abstract
The culture of embryos in the non-essential amino acid L-proline (Pro) or its analogues pipecolic acid (PA) and L-4-thiazolidine carboxylic acid (L4T) improves embryo development, increasing the percentage that develop to the blastocyst stage and hatch. Staining of 2-cell and 4-cell embryos with [...] Read more.
The culture of embryos in the non-essential amino acid L-proline (Pro) or its analogues pipecolic acid (PA) and L-4-thiazolidine carboxylic acid (L4T) improves embryo development, increasing the percentage that develop to the blastocyst stage and hatch. Staining of 2-cell and 4-cell embryos with tetramethylrhodamine methyl ester and 2′,7′-dichlorofluorescein diacetate showed that the culture of embryos in the presence of Pro, or either of these analogues, reduced mitochondrial activity and reactive oxygen species (ROS), respectively, indicating potential mechanisms by which embryo development is improved. Inhibition of the Pro metabolism enzyme, proline oxidase, by tetrahydro-2-furoic-acid prevented these reductions and concomitantly prevented the improved development. The ways in which Pro, PA and L4T reduce mitochondrial activity and ROS appear to differ, despite their structural similarity. Specifically, the results are consistent with Pro reducing ROS by reducing mitochondrial activity while PA and L4T may be acting as ROS scavengers. All three may work to reduce ROS by contributing to the GSH pool. Overall, our results indicate that reduction in mitochondrial activity and oxidative stress are potential mechanisms by which Pro and its analogues act to improve pre-implantation embryo development. Full article
(This article belongs to the Special Issue Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II)
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16 pages, 2034 KiB  
Article
Oocyte-Specific Deletion of Slc6a9 Encoding the GLYT1 Glycine Transporter Eliminates Glycine Transport in Mouse Preimplantation Embryos and Their Ability to Counter Hypertonic Stress
by Allison K. Tscherner, Taylor McClatchie, Gracia Kaboba, Detlev Boison and Jay M. Baltz
Cells 2023, 12(20), 2500; https://doi.org/10.3390/cells12202500 - 21 Oct 2023
Cited by 2 | Viewed by 1281
Abstract
Early preimplantation mouse embryos are sensitive to increased osmolarity, which can block their development. To overcome this, they accumulate organic osmolytes to maintain cell volume. The main organic osmolyte used by early mouse embryos is glycine. Glycine is transported during the mature egg [...] Read more.
Early preimplantation mouse embryos are sensitive to increased osmolarity, which can block their development. To overcome this, they accumulate organic osmolytes to maintain cell volume. The main organic osmolyte used by early mouse embryos is glycine. Glycine is transported during the mature egg and 1-cell to 4-cell embryo stages by a transporter identified as GLYT1, encoded by the Slc6a9 gene. Here, we have produced an oocyte-specific knockout of Slc6a9 by crossing mice that have a segment of the gene flanked by LoxP elements with transgenic mice expressing iCre driven by the oocyte-specific Gdf9 promoter. Slc6a9 null oocytes failed to develop glycine transport activity during meiotic maturation. However, females with these oocytes were fertile. When enclosed in their cumulus-oocyte complex, Slc6a9 null oocytes could accumulate glycine via GLYT1 transport in their coupled cumulus cells, which may support female fertility in vivo. In vitro, embryos derived from Slc6a9 null oocytes displayed a clear phenotype. While glycine rescued complete preimplantation development of wild type embryos from increased osmolarity, embryos derived from null oocytes failed to develop past the 2-cell stage even with glycine. Thus, Slc6a9 is required for glycine transport and protection against increased osmolarity in mouse eggs and early embryos. Full article
(This article belongs to the Special Issue Molecular and Clinical Advances in Understanding Early Embryo Development—Volume II)
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